1. 12-lead EKG Interpretation
Jamie Shedden, MSN, ACNP-BC

2. 12 Lead EKG Interpretation Objectives
Upon Completion of this program, the participant will be able to:
Successfully interpret the 12-lead EKG using a systematic evaluation of key components
Identify EKG rate and rhythm
Assess PR interval, QRS interval and QT interval with identification of significant abnormalities
Determine EKG Axis with identification of significant abnormalities
Successfully identify 12 lead EKG abnormalities and identify significance
Differentiate between significant 12 lead EKG changes
Identify EKG abnormalities related to artifact and lead misplacement

3. 12 Lead EKG Interpretation: Electrode Placement

4. 12 Lead EKG Interpretation Identification of Key Components
Determine rAte
Determine rHythm
Measure Intervals and Identify abnormalities
PR Intervals--AV Blocks, WPW
QRS Interval--Bundle Branch Blocks-RBBB, LBBB, IVCD
QT Interval--Long QT interval, Long QT Syndrome
Determination of Axis
Normal Axis, Left Axis Deviation, Right Axis Deviation and Indeterminate Axis
Hypertrophy
Diagnosis of chamber enlargement
Infarct
Assessment of significant QRST changes
Recognition of acute changes on the EKG (ischemia, injury or infarction)
Recognition of significant EKG abnormalities related to:
Electrolyte disturbances
Pericarditis
Medication effects
Lead misplacement and Artifact

5. 12 Lead EKG Interpretation Rate Determination
Numerous methods for rate determination
One easy “eyeball” method
Remember the pneumonic “ ”
Find the QRS complex closest to the dark vertical line on the EKG paper
Count forward or backward to the next QRS complex using the pneumonic
Estimate the HR based on where the next QRS complex falls in the count

6. 12 Lead EKG Interpretation Rhythm Determination
4 key questions of rhythm Analysis
Are there P waves?
Is the QRS wide or narrow?
Is the rhythm regular?
Who’s married to Whom?
(is the P related to the QRS?)

7. 12 Lead EKG Interpretation Rhythm Determination
Determinants of Sinus rhythm
P wave will be upright in Lead II {IF the P wave is NOT upright in Lead II, it is not sinus rhythm} Exceptions: Dextrocardia or lead reversal
Heart rate will be between bpm
Rhythm will be regular
If the P wave is upright in lead II but either rate or regularity is lacking, consider other sinus rhythms such as:
Sinus bradycardia—heart rate <60
Sinus tachycardia—heart rate >100
Sinus arrhythmia—rhythm irregular

8. 12 Lead EKG Interpretation Practice EKG
57 yo male with Hx of CAD, currently asymptomatic.
Rate—56
Rhythm—sinus bradycardia
Intervals—normal
Axis—Normal
Hypertrophy—None
QRST—Q wave in II, III, aVF
Impression—Sinus Bradycardia, Old Inferior Infarct

9. 12 Lead EKG Interpretation Rhythm Determination
Supraventricular Rhythms
Atrial Fibrillation/Atrial Flutter (most common)
MAT (Multifocal Atrial Tachycardia): definite P waves that appear different and irregular rhythm; wandering atrial pacemaker
PSVT or AVNRT: rate bpm; atrial activity not evident; sudden onset
Junctional rhythms: Escape rhythms occur when SA node fails to initiate the electrical impulse and another pacemaker assumes the function
AV nodal escape rhythm: rate between 40-60bpm; may or may not see negative P wave before the QRS in Lead II; QRS will be narrow unless there is other underlying abnormality of the ventricular conduction system
Accelerated junctional rhythm: rate 61-99bpm
Junctional tachycardia: rate >100bpm

10. Atrial Fibrillation Deviation from NSR
No organized atrial depolarization, so no normal P waves (impulses are not originating from the sinus node).
Atrial activity is chaotic (resulting in an irregularly irregular rate).
Uncoordinated atrial activation with consequent deterioration of atrial mechanical function; rapid fibrillatory waves that vary in amplitude, shape, and timing, irregular, frequently rapid ventricular response
Rapid,irregular sustained wide-QRS complex tachycardia strongly suggests AF with conduction over an accessory pathway or AF with BBB; extremely rapid rates >200 suggest accessory pathway or VT

11. Atrial Fibrillation
Etiology: theories suggest that it is due to multiple re-entrant wavelets conducted between the R & L atria. Either way, impulses are formed in a totally unpredictable fashion. The AV node allows some of the impulses to pass through at variable intervals (so rhythm is irregularly irregular).
May occur in isolation or in association with other arrhythmias, commonly atrial flutter or atrial tachycardia

12. Atrial Fibrillation

13. Atrial Flutter Deviation from NSR
No P waves. Instead flutter waves (note “sawtooth” pattern) are formed at a rate of bpm.
Only some impulses conduct through the AV node (usually every other impulse).

14. Atrial Flutter
Etiology: Reentrant pathway in the right atrium with every 2nd, 3rd or 4th impulse generating a QRS (others are blocked in the AV node as the node repolarizes).

15. Atrial Flutter

16. 12 Lead EKG Interpretation Rhythm Examples
Atrial Fibrillation
Multifocal Atrial Tachycardia or
Wandering atrial Pacemaker

17. Rhythm Examples

18. Rhythm Examples
Atrial Flutter

19. Rhythm Examples
Atrial Fibrillation

20. Rhythm Examples
Atrial Fluter

21. 12 Lead EKG Interpretation Rhythm Examples
Why is this not PSVT or AVNRT? Presence of obvious atrial activity and ventricular rate just at 150.
Remember to Think Atrial Flutter until proven otherwise.
ATRIAL FLUTTER

22. 12 Lead EKG Interpretation Rhythm Examples
Junctional Tachycardia (P wave negative following QRS complex)
Accelerated Junctional rhythm (P wave negative and precedes the QRS complex)
AV nodal escape rhythm (no evidence of atrial activity)

23. 12 Lead EKG Interpretation Rhythm Examples
Accelerated junctional rhythm—inverted P wave in lead II, rate , narrow complex QRS.

24. 12 Lead EKG Interpretation Rhythm Examples
Junctional bradycardia, no P wave obvious, narrow complex QRS, regular rhythm

25. 12 Lead EKG Interpretation Rhythm Examples
Junctional rhythm with retrograde P waves, inverted in lead II, rate 60 bpm, narrow complex QRS.

26. 12 Lead EKG Interpretation Rhythm Determination
Ventricular (Wide QRS) rhythms
Slow idioventricular escape rhythm: rate 30-40bpm; no P wave evident; wide QRS
Accelerated Idioventricluar rhythm: rate bpm
Ventricular Tachycardia: ventricular rate > bpm; wide QRS
Regular wide complex Tachycardia is always considered VT until proven otherwise
Ventricular Fibrillation: totally disorganized and chaotic ventricular rhythm
Premature Beats
PAC’s
PJC’s
PVC’s

27. 12 Lead EKG Interpretation Rhythm Examples
Idioventricular escape rhythm
Accelerated Idioventricular rhythm
Ventricular Tachycardia
Ventricular Fibrillation

28. 12 Lead EKG Interpretation Rhythm Examples

29. 12 Lead EKG Interpretation Rhythm Examples

30. 12 Lead EKG Interpretation Rhythm Examples
Monomophic Ventricular tachycardia

31. 12 Lead EKG Interpretation Rhythm Examples
PVCs; non-sustained ventricular tachycardia

32. 12 Lead EKG Interpretation Rhythm Examples
Torsades de pointes from too much sotalol
Torsades de pointes

33. 12 Lead EKG Interpretation Rhythm Examples
Ventricular tachycardia, terminated with Overdrive pacing
V. Fib with shock, unsuccessful

34. 12 Lead EKG Interpretation Rhythm Examples
Junctional Tachycardia (P wave negative following QRS complex)
Accelerated Junctional rhythm (P wave negative and precedes the QRS complex)
AV nodal escape rhythm (no evidence of atrial activity)

35. 12 Lead EKG Interpretation Rhythm Determination
Quick Review of Ventricular (Wide QRS) rhythms
Slow idioventricular escape rhythm: rate 30-40bpm; no P wave evident; wide QRS
Accelerated Idioventricluar rhythm: rate bpm
Ventricular Tachycardia: ventricular rate > bpm; wide QRS
Regular wide complex Tachycardia is always considered VT until proven otherwise
Ventricular Fibrillation: totally disorganized and chaotic ventricular rhythm
Premature Beats
PAC’s
PJC’s
PVC’s

36. 12 Lead EKG Interpretation Rhythm Examples
Idioventricular escape rhythm
Accelerated Idioventricular rhythm
Ventricular Tachycardia
Ventricular Fibrillation

37. 12 Lead EKG Interpretation Assessment of the PR Interval
Period that extends from the onset of atrial depolarization (beginning of the P wave) to the onset of ventricular depolarization (beginning of the QRS complex)
Best lead for measurement is Lead II
Normal range seconds

38. 12 Lead EKG Interpretation PR Interval Abnormalities
The Short PR Interval
Usually occurs when conduction occurs through an accessory pathway
Consider WPW syndrome characterized by short PR and delta wave
Other causes include accelerated conduction of the electrical activity or anatomic shortening of the AV node
Uncommon for PR to be short, more common for long PR interval

39. 12 Lead EKG Interpretation PR Interval Abnormalities

40. 12 Lead EKG Interpretation PR Interval Abnormalities
The Long PR Interval
Measures longer than seconds (longer than one large box on EKG paper)
First Degree AV block—delay of conduction to the ventricle across the AV node—clinically not significant
Second Degree AV Block—failure of at least some atrial impulses to conduct to the ventricles—includes Mobitz I, Mobitz II or 2:1 AV block
Third Degree AV Block—none of the atrial impulses are conducted to the ventricle—no relationship between P waves and QRS complexes

41. 12 Lead EKG Interpretation PR Interval Abnormalities

42. 12 Lead EKG Interpretation Assessment of the QRS Interval
Represents the time it takes for ventricular depolarization to occur
Normal QRS measures 0.10 seconds or less
Essential to examine all 12 leads and use the lead in which the QRS complex appears to be longest

43. 12 Lead EKG Interpretation Assessment of the QRS Interval
Only abnormality to consider is WIDE QRS complex
If the rhythm is determined to be sinus or supraventricular and the QRS is wide, systematic approach should then focus on the type of QRS widening (not to be considered in Ventricular tachycardia)

44. 12 Lead EKG Interpretation Diagnosis of Bundle Branch Block
3 Key leads used in the diagnosis of the type of BBB
Leads I and V6 are Left sided leads
Lead V1 is the single right sided lead
Normal Ventricular Depolarization—begins with left side of septum, then left and right ventricles are simultaneously activated

45. 12 Lead EKG Interpretation Diagnosis of RBBB
QRS widening of at least 0.11 sec
rSr’ or rsR’ in lead V1
Wide terminal S wave in leads I and V6
Considered incomplete RBBB if typical morphology but complex measures <0.11 sec

46. 12 Lead EKG Interpretation Diagnosis of LBBB
QRS widening of at least 0.12 sec
Upright (monophasic) QRS complex in leads I and V6
Predominantly negative QRS complex in lead V1
Incomplete LBBB is rare and difficult to recognize
IVCD diagnosis is simply ARS widening of >0.11 sec and neither typical RBBB nor typical LBBB presentation

47. 12 Lead EKG Interpretation Secondary ST-T Wave Changes in BBB
Orientation of the ST segment and the T wave with typical RBBB and LBBB should be opposite that of the last QRS deflection in each o the 3 key leads
Typical RBBB—Last QRS deflection is positive therefore, ST-T wave is negative in V1; last QRS deflection is negative and ST-T wave is positive in leads I and V6
Typical LBBB—Last QRS deflection is negative and ST-T wave is positive in V1; last QRS deflection is positive and ST-T wave is negative in Leads I and V6

48. 12 Lead EKG Interpretation Example EKG for Review
Systematic Approach 1)no definite P waves present 2)QRS is wide 3)rhythm is irregular 4)there is not relationship
DX: Atrial Fibrillation Next dx QRS widening Lead V1 has rsR’, positive QRS deflection with negative ST-T wave Lead I and V6 have wide terminal S wave (particularly lead I), negative QRS deflection and positive ST-T wave

49. 12 Lead EKG Interpretation Clinical Significance of BBB
If found in asymptomatic adult in ambulatory setting, clinical significance is minimal except for increasing likelihood that underlying heart disease is present
Does this patient need a pacemaker? The chance of developing complete AV block and therefore need for PPM is quite small in asymptomatic individuals
Acute development of BBB may be associated with Acute infarction and therefore the chance of developing Complete AV block is substantial and Pacing may be required
Diagnosis of Myocardial Infarction with BBB is difficult, particularly LBBB which essentially precludes the diagnosis. There are 2 exceptions: if Q wave is seen in I or V6, consider old infarct or if primary ST-T wave changes are present, consider ischemia or infarction

50. 12 Lead EKG Interpretation Example EKG for Review

51. 12 Lead EKG Interpretation Example EKG for Review

52. 12 Lead EKG Interpretation Assessment of the QT Interval
QT interval is the period from the beginning of ventricular depolarization until the end of ventricular repolarization—measured from the onset of the Q wave (or R wave if Q not present) to the end of the T wave
Measure QT in a lead where terminal boundary of the T wave is clear
QT interval may be short, normal or long. Short QT interval is difficult to distinguish from normal QT. Focus should be on Normal or Long QT interval
For heart rate of 60 bpm, upper limit normal QT is sec

53. 12 Lead EKG Interpretation Assessment of the QT Interval
QT interval is affected by heart rate, age and sex of the individual
QTc is the correction made for heart rate, what the QT interval should measure at a heart rate of 60 bpm
Determination of QTc is complex, most 12 lead readings give a QTc
Precise determination of the QTc is usually not necessary
Use General rule for measurement
QT interval should not measure more than half of the R-R interval
General rule is not valid if heart rate is >100 and QT interval has little clinical meaning at this point
Borderline QT interval—if interval is approximately half of the R-R interval
Normal Abnormal

54. 12 Lead EKG Interpretation Common Causes of Prolonged QT
Drugs
Type IA Antiarrhythmic agents (I.e., quinidine, procainamide, disopyramide
Type III Antiarrhythmic agents (Amiodarone, Sotalol)
Tricyclic antidepressants
Phenothiazines
Electrolytes
Hypokalemia
Hypomagnesemia
Hypocalcemia
CNS Catastrophe
Stroke
Intracerebral or brainstem bleeding
Coma
Seizures
Bundle Branch Block or IVCD
Ischemia or Infarction
BBB and Ischemia or infarction are identified by other characteristics and QT is not usually a diagnostic criteria
Other causes—QT may be the only clinical finding to suggest the abnormality

55. 12 Lead EKG Interpretation Practice EKG
Systematic Approach: 1) Definite P waves, positive in lead II 2) QRS is normal 3) rhythm is regular, rate approx ) relationship btwn QRS and P present ) PR interval normal 6) QT normal (less than half R-R) 7)Axis—lead I positive, aVF net negative, lead II net negative=LAD (pathologic)
Diagnosis: Normal Sinus rhythm, LAD

56. 12 Lead EKG Interpretation Practice EKG
70 yo wm with new onset chest pain, NPT
Sinus rhythm with complete LBBB with typical secondary ST-T wave changes with LBBB

57. 12 Lead EKG Interpretation Practice EKG
Systematic Approach: 1) Definite P waves, positive in lead II 2) QRS is normal 3) rhythm is regular, rate approx ) relationship btwn QRS and P present ) PR interval normal 6) QT normal (less than half R-R) 7)Axis—lead I positive, aVF net negative, lead II net negative=LAD (pathologic)
Diagnosis: Normal Sinus rhythm, LAD

58. 12 Lead EKG Interpretation Practice EKG
49 yo black male with long-standing HTN
Sinus rhythm, RAE (p wave in II), LAE (negative component of P wave in V1), LVH with strain vs. ischemia (need comparison tracing)

59. 12 Lead EKG Interpretation Practice EKG
Rate—
Rhythm—
Intervals—
Axis—
Hypertrophy—
QRST—
Impression—

60. 12 Lead EKG Interpretation Electrolyte Disturbances—Hyperkalemia
Hallmark for diagnosis is tall, peaked T waves with narrow base
T wave prominence may be normal repolarization variant, tend to be less pointed with broader base
Ischemia should also be considered with tall peaked T waves in anterior leads, rule out posterior wall ischemia with mirror test (changes with hyperkalemia usually diffuse)
Can use EKG to verify initial hyperkalemia findings on lab while waiting on repeat testing

61. 12 Lead EKG Interpretation Electrolyte Disturbances—Hypokalemia
Characteristic sign is the development of U waves predominantly seen in leads V2 through V5
EKG is not a reliable tool for assessing the presence of severity of hypokalemia
Similar EKG changes may be present with hypomagnesemia
Both disorders should be considered when these EKG changes are present

62. 12 Lead EKG Interpretation Electrolyte Disturbances
Hypercalcemia
May shorten the QT interval
Difficult to recognize
Changes are usually not noticeable until serum calcium elevation is marked
Hypocalcemia
May lengthen the QT interval usually without affecting the ST segment or T wave morphology, can cause Torsades
Hypernatremia and Hyponatremia
Not associated with any EKG changes

63. 12 Lead EKG Interpretation Hypothermia
Everything slows down—bradycardia and possible prolongation of intervals
J wave or Osborne wave—distinctive and virtually diagnostic ST segment elevation, abrupt ascent right at the J point and then a sudden plunge back to baseline
Various arrhythmias, Slow Atrial Fib most common
Artifact from muscle tremor

64. 12 Lead EKG Interpretation Pericarditis
Diagnosed with history, Physical exam and EKG findings
Characteristic symptom is chest pain that may is usually pleuritic and increases with inspiration
Physical exam may reveal pericardial friction rub
EKG findings usually occur in 4 stages
Stage I—generalized ST segment elevation
Stage II—transitional stage, pseudonormalization
Stage III—generalized T wave inversion
Stage IV—normalization
EKG findings in Stage I may be confused with J point elevation of early repolarization or acute infarction, History and PE is essential

65. 12 Lead EKG Interpretation Pericarditis
Stage I Stage III

66. 12 Lead EKG Interpretation Pericarditis

67. 12 Lead EKG Interpretation Medication Effects
Digitalis—Therapeutic or toxic?
Digitalis Effect –scooped appearance or gradual downslope of the ST segment, ST segment depression with flattening or inversion of the T wave
Digitalis effect is normal and predictable, does not necessitate discontinuing the drug, may only be seen in about 60% of patients

68. 12 Lead EKG Interpretation Medication Effects
Digitalis—Therapeutic or toxic?
Digoxin Toxicity can cause
AV conduction abnormalities
Tachyarrhythmias—enhances automaticity, Paroxysmal atrial tachycardia and PVCs are most common, junctional rhythms common
Sinus node suppression (sinus exit block)
Most characteristic rhythm disturbance of dig toxicity is PAT with second-degree AV block

69. 12 Lead EKG Interpretation Practice EKG
Digoxin effects on ST segment, sloping ST segment

70. 12 Lead EKG Interpretation Lead Misplacement Most common problem is interchanging the left and right arm electrodes which reverses the polarity of the QRS complex in the six standard leads
Clues to diagnosis of lead misplacement
P wave in lead II is inverted
global negativity in lead I
QRS complex in aVR is upright
DX: reversal of L and R arm electrodes

71. 12 Lead EKG Interpretation Lead Misplacement
Normal R wave progression Precordial lead placement one interspace too high causes loss of R wave and appearance of anterior infarct

72. 12 Lead EKG Interpretation Practice EKG
Healthy 55 yo male without symptoms, no medications
Rate—just under 60
Rhythm—P waves present and upright in lead II, QRS is narrow, rhythm regular, definite relationship—sinus bradycardia
Intervals—normal
Axis—normal, approx deg
Hypertrophy—meets voltage criteria for LVH
QRST—tiny Q waves in multiple leads, rSr’ pattern in V1, early transition, tall prominent t waves with narrow base in anterolateral leads, ST segment is isoelectric
Impression—sinus bradycardia, other changes not clinically significant in healthy asymptomatic patient, prominent T waves most likely represent normal repolarization variant

73. 12 Lead EKG Interpretation Practice EKG
Systematic Approach: 1)P waves are present 2)QRS is normal 3)rhythm is regular 4)no relationship of QRS to P 5) PR interval inconsistent 6)QT normal ) Axis—lead I positive, aVF positive=normal axis
DX: Complete Heart block